Activins are pluripotent hormones/growth factors that belong to the TGF-β superfamily of growth and differentiation factors. They play a role in cell growth, differentiation and apoptosis, endocrine function, metabolism, wound repair, immune responses, homeostasis, mesoderm induction, bone growth and many other biological processes. Activins and the related bone morphogenic proteins (BMPs) transduce their signal through two classes of single transmembrane receptors. The receptors possess intracellular serine/threonine kinase domains. Signaling occurs when the constitutively active type II kinase domain phosphorylates the type I receptor, which upon activation phosphorylates intracellular signaling molecules. To generate antagonistic ligands, we generated chimeric molecules that disrupt the receptor interactions and thereby the phosphorylation events. The chimeras were designed based on available structural data to maintain high affinity binding to type II receptors. The predicted type I receptor interaction region was replaced by residues present in inactive homologs or in related ligands with different type I receptor affinities.
ExtractPermanent brain damage commonly follows asphyxia in the newborn period. A clinical survey of 287 newborn infants with seizures indicated that an elevation of levels of phosphorus in serum was not uncommonly associated with the subsequent demonstration of cerebral damage. Experiments were undertaken to examine the possible relations between these variables.Newborn rats were placed for 20 minutes in a chamber, which was continuously flushed with nitrogen and contained less than 0.1% oxygen (micro Scholander and gas-liquid chromatography). During this period they became cyanotic and made gasping respiratory movements. Serial measurements of levels of calcium, phosphorus and urea nitrogen in serum were made after the rats were removed from the chamber. In comparison with the litter-mate controls, animals subjected to the insult had a significant transient elevation in phosphorus levels 24 hours after the insult (table I). Calcium and urea nitrogen levels were unchanged. There was no histological evidence of renal damage. Subsequently, the experimental rats grew more slowly than their litter mates (table III) and demonstrated more apprehensive behavior. The survivors were killed at 10 weeks of age and the glycolipid N-acetylneuraminic acid (NANA) levels were determined in extracts of cerebral hemispheres. In the experimental animals, the glycolipid NANA content of brain was reduced to 1.90 ±0.10/^moles/g wet weight (normal 2.13 ±0.09), although the total weight and cholesterol content of cerebral hemispheres did not differ between the two groups. Speculation
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